Question

Comparison of Cardiovascular Exemplars:

	Angina	Acute Myocardial Infarction
Pathophysiology
Etiology
Assessment Findings (including a minimum of 1 Diagnostic test per column)
Nursing Diagnosis (minimum of 2 for each)
Interventions (minimum of 5 for each) (including meds and Surgical interventions)

NUR2790 Professional Nursing III

Module 7 Written Assignment – Simulation

Student Name:___________________________________________________________________

Module 07

Scoring Rubric: Cardiovascular Exemplars

Criteria	Points
Include Pathophysiology for each exemplar.	1
Identify possible causes for each exemplar.	1
List assessment findings, and a minimum of 1 diagnostic test for each exemplar.	1
Include 2 possible Nursing Diagnoses for each exemplar.	2
List a minimum of 5 possible interventions for each exemplars.	1
Total	6

Answer 1

ANGINA

Angina pectoris is a clinical syndrome usually charecterized by episodes of paroxysms of pain or pressure in the anterior chest.

Pathophysiology

Angina is usually caused by atherosclerotic disease. Almost invariobly,angina is associated with a significant obstruction of atleast one major coronary artery. Normally ,the myocardium extracts a large amount of oxygen by the coronary circulation.to meets its continous demands. When there is an increased demands,flow through the coronary arteries need to increased.When there is blockage in a coronary artery,the flow can not be increased, and ischemias results.

Etiology

• Insufficient coronary blood flow resulting in a decreased oxygen supply when there is an increased myocardial demand for oxygen in response to physical exertion or emotional stress.t

Diagnostic tests

• History related to clinical manifestations of ischemia
• 12 lead ECG may show changes indicating of ischemia such as T wave inversiion
• CRP and cardiac boiomarker values to rule out ACS
• Excercise or pharmacologic stress test in which heart is monitered by ECG.
• Nuclear scan.

Nursing diagnosis

1.Acute pain related to decreased myocardial blood flow and Increased cardiac workload/oxygen consumption

Possibly evidenced by

• Reports of pain varying in frequency, duration, and intensity (especially as condition worsens)
• Narrowed focus
• Distraction behaviors (moaning, crying, pacing, restlessness)
• Autonomic responses, e.g., diaphoresis, blood pressure and pulse rate changes, pupillary dilation, increased/decreased respiratory rate

Desired Outcomes

• Report anginal episodes decreased in frequency, duration, and severity.
• Demonstrate relief of pain as evidenced by stable vital signs, absence of muscle tension and restlessness

nursing intervensions

1.Instruct patient to notify nurse immediately when chest pain occurs.

2.Assess and document patient response to medication.

3.Identify precipitating event, if any: frequency, duration, intensity, and location of pain.

4.Observe for associated symptoms: dyspnea, nausea and vomiting, dizziness, palpitations, desire to micturation

5.Evaluate reports of pain in jaw, neck, shoulder, arm, or hand (typically on left side).

6.Place patient at complete rest during anginal episodes.

7.Elevate head of bed if patient is short of breath

8.Monitor heart rate and rhythm.

9.Monitor vital signs every 5 min during initial anginal attack

10.Maintain quiet, comfortable environment. Restrict visitors as necessary

11.Maintain quiet, comfortable environment. Restrict visitors as necessary

12.Provide supplemental oxygen as indicated.

13.Administer antianginal medication(s) promptly as indicated:

• Nitroglycerin: sublingual (Nitrostat), buccal, or oral tablets, metered-dose spray.

MYOCARDIAL INFARCTION

DEFINITION-

Myocardial infarction is defined as myocardial necrosis in a clinical setting consistent with myocardial ischemia (1). These conditions can be satisfied by a rise of cardiac biomarkers (preferably cardiac troponin [cTn]) above the 99th percentile of the upper reference limit (URL) plus at least one of the following:

• Symptoms of ischemia

• ECG changes indicative of new ischemia (significant ST/T changes or left bundle branch block)

• Development of pathologic Q waves

• Imaging evidence of new loss of myocardium or new regional wall motion abnormality

• Angiography or autopsy evidence of intracoronary thrombus

Etiology

• Type 1: Spontaneous MI caused by ischemia due to a primary coronary event (eg, plaque rupture, erosion, or fissuring; coronary dissection)

• Type 2: Ischemia due to increased oxygen demand (eg, hypertension), or decreased supply (eg, coronary artery spasm or embolism, arrhythmia, hypotension)

• Type 3: Related to sudden unexpected cardiac death

• Type 4a: Associated with percutaneous coronary intervention (signs and symptoms of myocardial infarction with cTn values > 5 × 99th percentile URL)

• Type 4b: Associated with documented stent thrombosis

• Type 5: Associated with coronary artery bypass grafting (signs and symptoms of myocardial infarction with cTn values >10 × 99th percentile URL)

PATHOPHYSIOLOGY

MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria.

Right ventricular infarction usually results from obstruction of the right coronary or a dominant left circumflex artery; it is characterized by high RV filling pressure, often with severe tricuspid regurgitation and reduced cardiac output.

An inferoposterior infarction causes some degree of RV dysfunction in about half of patients and causes hemodynamic abnormality in 10 to 15%. RV dysfunction should be considered in any patient who has inferoposterior infarction and elevated jugular venous pressure with hypotension or shock. RV infarction complicating LV infarction significantly increases mortality risk.

Anterior infarcts tend to be larger and result in a worse prognosis than inferoposterior infarcts. They are usually due to left coronary artery obstruction, especially in the anterior descending artery; inferoposterior infarcts reflect right coronary or dominant left circumflex artery obstruction.

Infarct extent

Infarction may be

• Transmural

• Nontransmural

Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG.

Nontransmural (including subendocardial) infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities. Sub endocardial infarcts usually involve the inner one third of myocardium, where wall tension is highest and myocardial blood flow is most vulnerable to circulatory changes. These infarcts may follow prolonged hypotension.

Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG. Volume of myocardium destroyed can be roughly estimated by the extent and duration of CK elevation or by peak levels of more commonly measured cardiac troponins.

Non–ST-segment elevation myocardial infarction (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or troponin T and CK will be elevated) without acute ST-segment elevation. ECG changes such as ST-segment depression, T-wave inversion, or both may be present.

ST-segment elevation myocardial infarction (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin. Troponin I or troponin T and CK are elevated.

Nursing diagnosis

1.Acute pain related to tissue ischemia (coronary artery occlusion)

interventions

Monitor and document characteristic of pain, noting verbal reports, nonverbal cues (moaning, crying, grimacing, restlessness, diaphoresis, clutching of chest) and BP or heart rate changes.

Obtain full description of pain from patient including location, intensity (using scale of 0–10), duration, characteristics (dull, crushing, described as “like an elephant in my chest”), and radiation. Assist patient to quantify pain by comparing it to other experiences.

Instruct patient to report pain immediately. Provide quiet environment, calm activities, and comfort measures. Approach patient calmly and confidently

Instruct patient to do relaxation techniques: deep and slow breathing, distraction behaviors, visualization, guided imagery. Assist as needed.

Check vital signs before and after narcotic medication.

Administer supplemental oxygen by means of nasal cannula or face mask, as indicated.

Administer medications as indicated:

Antianginals: nitroglycerin (Nitro-Bid, Nitrostat, Nitro-Dur), isosorbide dinitrate (Isordil), mononitrate (Imdur)

Beta-blockers: atenolol (Tenormin), pindolol(Visken), propranolol (Inderal), nadolol (Corgard), metoprolol (Lopressor)

Analgesics: morphine, meperidine (Demerol)

2. Activity intolerance related to Imbalance between myocardial oxygen supply and demand

interventions

Document heart rate and rhythm and changes in BP before, during, and after activity. Correlate with reports of chest pain or shortness of breath

Encourage rest initially. Thereafter, limit activity on basis of pain and/or adverse cardiac response. Provide nonstress diversional activities.

Instruct patient to avoid increasing abdominal pressure (straining during defecation).

Explain pattern of graded increase of activity level: getting up to commode or sitting in chair, progressive ambulation, and resting after meals.

Review signs and symptoms reflecting intolerance of present activity level or requiring notification of nurse or physician.